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阻断(体内的)异黄酮化学感受器以预防疾病。 (注:原文“in to”表述有误,推测应该是“in vivo”之类表示在体内的意思,这里按照合理推测补充完整后翻译)

Blocking the isoflavone chemoreceptor in to prevent disease.

作者信息

Ji Peiyun, Bao Yazhou, Zhou Hao, Pei Yong, Song Wen, Ou Kangmiao, Qiao Zijin, Si Jierui, Zhong Zengtao, Xu Xia, Huang Tao, Shen Danyu, Yin Zhiyuan, Dou Daolong

机构信息

Department of Plant Pathology, Nanjing Agricultural University, Nanjing 210095, China.

Academy for Advanced Interdisciplinary Studies, Nanjing Agricultural University, Nanjing 210095, China.

出版信息

Sci Adv. 2025 Jan 10;11(2):eadt0925. doi: 10.1126/sciadv.adt0925. Epub 2025 Jan 8.

Abstract

Inhibiting pathogen chemotaxis is a promising strategy for reducing disease pressure. However, this strategy is currently in the proof-of-concept stage. Here, was used as a model, as its biflagellated zoospores could sense genistein, a soybean root exudate, to navigate host and initiate infection. We identify IRK1 (isoflavone-insensitive receptor kinase 1) as a receptor for genistein, with PsIRK2 functioning as a coreceptor that enhances the binding affinity of PsIRK1 to genistein and regulates chemotaxis by phosphorylating G protein α subunit. Last, we identify an antagonist, esculetin, which disrupts the PsIRK1-genistein interaction, thereby preventing infection by repelling zoospores. Our findings reveal the mechanism by which senses host genistein and demonstrate a strategy for disease prevention by targeting the chemoreceptor.

摘要

抑制病原体趋化性是减轻疾病压力的一种有前景的策略。然而,这一策略目前正处于概念验证阶段。在此,以[具体病原体名称]为模型,因为其双鞭毛游动孢子能够感知大豆根分泌物染料木黄酮,从而导航至宿主并引发感染。我们鉴定出IRK1(异黄酮不敏感受体激酶1)为染料木黄酮的受体,PsIRK2作为共受体发挥作用,增强PsIRK1与染料木黄酮的结合亲和力,并通过磷酸化G蛋白α亚基来调节趋化性。最后,我们鉴定出一种拮抗剂七叶亭,它破坏PsIRK1 - 染料木黄酮的相互作用,从而通过排斥游动孢子来防止[具体病原体名称]感染。我们的研究结果揭示了[具体病原体名称]感知宿主染料木黄酮的机制,并展示了一种通过靶向化学感受器进行疾病预防的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c8c/11708900/54f25b9abd9e/sciadv.adt0925-f1.jpg

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